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Basilar artery thrombosis in a 20-year-old pregnant patient – difficulties in establishing the aetiology
Piotr F. Czempik
Department of Anaesthesiology and Intensive Care, School of Medicine in Katowice, Medical University of Silesia in Katowice, Poland
LISTY DO REDAKCJI
Anestezjologia Intensywna Terapia 2019; 51, 4: 336–338
ADRES DO KORESPONDENCJI:
Piotr F. Czempik, Department of Anaesthesiology and Intensive Care, School of Medicine in Katowice, Medical University of Silesia in Katowice, 14 Medyków St., 40-752 Katowice, Poland, e-mail: pczempik@sum.edu.pl Dear Editor,
I would like to present a case of a 20-year-old pregnant patient with basilar artery thrombosis and our struggle to establish its aetiology in this particular patient.
Pregnancy constitutes a risk factor for both arterial and venous cerebral thrombosis. The reported incidence of ischaemic stroke in young adults is 10.8/100,000/year [1]. During pregnan- cy the incidence of ischaemic stroke is estimated at 12.2/100,000 pregnancies [2]. The most common causes of non- haemorrhagic stroke in pregnancy are cardioembolism, coagulopathy and preeclampsia/eclampsia. Nevertheless, establishing the aetiology of stroke in pregnancy can be challenging.
A 20-year-old pregnant patient in the 8th week of gestation was ad- mitted to Department of Anaesthe- siology and Intensive Care (ICU) of a tertiary medical centre following ischaemic stroke of the left cerebellar hemisphere. The patient was initially admitted to emergency department (ER) of a district general hospital with symptoms of headache, vertigo and impaired balance. These symptoms were present from the morning hours of the previous day, however the pa- tient did not seek medical attention at that time. On admission to ER the patient was alert, non-responsive, meningeal signs were negative, pupils were equal, right 3rd cranial nerve pa- resis was present, vertical movements of eyeballs were observed, flexion of right limbs and extension of left limbs to pain was elicited and the Babinski sign was present bilaterally. Due to the risk of aspiration, the patient was
intubated and mechanical ventilation was commenced. Computed tomogra- phy (CT) revealed a 9 mm thrombus in the basilar artery and signs of left cer- ebellar hemisphere ischaemia. Head and neck angio-CT confirmed a throm- bus in the basilar artery with no signs of vertebral artery dissection. Medi- cal and drug history were negative.
The patient underwent uncomplicated caesarean section 3 years earlier. Fam- ily history revealed very short height in the mother and grand mother. On admission to ICU the neurological sta- tus of the patient did not change com- pared to initial evaluation. Both neu- rological and interventional radio logy consultations were requested, however the patient was disqualified from intra- venous thrombolysis and percutane- ous thrombectomy due to late presen- tation (over 24 hrs). Medical treatment of cerebral oedema was commenced (mannitol) and the patient was started on antiplatelet (acetylsalicylic acid 150 mg) and anticoagulant (dalteparin 200 IU kg-1) medication. The ultrasound (US) examination revealed uterus cor- responding to 10 weeks of gestation, gestational vesicle with a foetus cor- responding to 9 weeks of gestation, normal foetus heart beat and normal decidual-chorionic reaction. Repeat head CT examination on day 4 con- firmed ischaemia of left cerebellar hemisphere, upper part of pons, left cerebral peduncle, moderate oedema of cerebellum and brainstem, lower intensity of hyperdense signal in the basilar artery. On day 5 the patient re- gained consciousness, started open- ing eyes to voice, however was not fol- lowing commands. On day 13 repeat
Należy cytować anglojęzyczną wersję: Czempik PF. Basilar artery thrombosis in a 20-year-old pregnant patient – difficulties in establishing the aetiology. Anaesthesiol Intensive Ther 2019; 51, 4: 330–332. doi: https://doi.org/10.5114/ait.2019.87329
337 Basilar artery thrombosis in a 20-year-old pregnant patient – difficulties in establishing the aetiology
head CT revealed reduced ischaemic area, reduced cerebellar oedema, and lower intensity of hyperdense signal in the basilar artery. On day 18, after receiving a consent from the court of law, dilatational percutaneous tracheostomy (Griggs method) was performed, respiratory support was gradually decreased and the wean- ing process was completed on day 21.
On day 22 neurological rehabilita- tion consultation was requested and confirmed bulbar syndrome with dys- phagia, immobile tongue, diminished palatine-pharyngeal reflexes, quad- riplegia and suspicion of locked-in syndrome. Due to the risk of aspiration and need for prolonged enteral nutri- tion, percutaneous gastrostomy was inserted on day 32.
DIFFERENTIAL DIAGNOSIS, INVESTIGATIONS AND TREATMENT
Along with usual treatment and management of the patient, efforts were undertaken to find the cause of basilar artery thrombosis. The initial evaluation included an echocardio- graphic examination – no interatrial septum defect or thrombus were de- tected. US Doppler of lower extremi- ties was also normal. After cardiac abnormalities and arterial dissection were ruled out, the next most likely cause of thrombosis was unspecified coagulopathy. The initial evaluation of this suspected coagulopathy includ- ed the standard laboratory coagulation panel (Table 1) and antiphospholipid syndrome panel (Table 2).
The results of standard labora- tory coagulation tests were normal with the exception of mildly elevated D-dimers (1711 ng mL-1). The results of the antiphospholipid syndrome panel were also negative. The last step in establishing the cause of thrombosis was determination of activity of pro- tein C, free protein S, anti-thrombin, factor V Leiden and prothrombin gene 20210A mutation, homocysteine con- centration, activity of factor VIII, IX, XI and plasminogen – the results are presented in Table 3. Determinations of these coagulation and anticoagula- tion factors were performed 4 weeks
after presentation in order to obtain the most objective results.
Activity levels of coagulation factor VIII and IX were moderately and mildly elevated, but activity increased to such a degree is normal during physiologic pregnancy. The diagnostic imaging and laboratory tests performed did not reveal the cause of ischae mic stroke in this particular patient.
The patient gradually started mo- bilizing upper and lower extremities, communication with the patient was maintained through nonverbal mea- sures. In the 14th week of pregnancy the patient was transferred to De- partment of Neurological Rehabilita- tion. Haematology consultation was requested and as the final diagnostic step, histological examination of bone marrow and tests for Janus kinase 2 mutation and paroxysmal nocturnal haemoglobinuria were suggested.
The presented case report de- scribes a basilar artery thrombosis in a young, apparently healthy, pregnant patient. There is increasing incidence of stroke in younger patients [3]. Al- though strokes in young adults are less frequent than in older patients,
TABLE 1. Standard laboratory coagulation panel Parameter Value Reference
range Prothrombin time (s) 12.6 9.4–12.5
INR 1.11 0.80–1.20
Prothrombin activity (%) 85 80–120 Fibrinogen (mg dL-1) 314 200–393
aPTT (s) 28.1 25.4–36.9
D-dimers (ng mL-1) 1711 < 500 Platelets (G L-1) 290 130–400
aPTT – activated partial thromboplastin time, INR – international normalised ratio
when faced with acute neurologic symptoms in this age group, stroke should be considered in differential diagnosis. In our case the patient was not a candidate for thrombolysis/
thrombectomy due to late presenta- tion, what significantly impacted on neurologic recovery of the patient.
There is high variability in aetiol- ogy of stroke in this population [4].
There is also a wide variety of uncom- mon causes of stroke in young pa- tients. This variability is even higher in pregnant patients, as pregnancy is associated with several additional risk factors for stroke, particularly TABLE 2. Antiphospholipid syndrome laboratory panel
Parameter Value Reference range
Lupus anticoagulant 0.76 0.80–1.20
β2-glycoprotein I IgM (RU mL-1) 6.32 < 20 negative result β2-glycoprotein I IgG (RU mL-1) < 2 < 20 negative result
Anti-cardiolipin antibody IgM (MPLU mL-1) 1.7 < 12
Anti-cardiolipin antibody IgG (GPLU mL-1) 2.9 < 12
IgG – immunoglobulin class G, IgM – immunoglobulin class M
TABLE 3. Additional laboratory panel
Parameter Result Reference range
Protein C activity (%) > 149.9 70–140
Protein S free (%) ELISA 66 64–126
Anti-thrombin activity (%) 118 75–120
Factor V Leiden mutation Negative –
Prothrombin gene 20210A mutation Negative –
Homocysteine (µmol L-1) CMIA 5.36 4.44–13.56
Factor VIII activity (%) 212.1 70–150
Factor IX activity (%) 130.3 70–120
Factor XI activity (%) 115.7 65–150
Plasminogen (%) 152 80–120
CMIA – chemiluminescent magnetic microparticle immunoassay, ELISA – enzyme-linked immunosorbent assay
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Piotr F. Czempik
preeclampsia/eclampsia, reversible cerebral vasoconstriction syndrome and cerebral venous sinus thrombo- sis [5]. Physiologic changes attribu- tive to pregnancy might predispose to stroke, particularly dehydration, haemoconcentration or upregula- tion of clotting factors. Despite more accurate diagnostic tools becoming available, the most common type of stroke in young patients is a stroke of undetermined aetiology [6].
CONCLUSIONS
When faced with pregnant patients presenting with acute neurologic de- terioration one should always con- sider stroke in a differential diagnosis.
Prompt diagnosis and treatment is crucial for satisfactory neurological re- covery. Establishing aetiology of stroke in this population is challenging and often remains undetermined due to numerous possible causes.
ACKNOWLEDGEMENTS
1. Financial support and sponsorship:
none.
2. Conflict of interest: none.
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